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PubMed1992

Aggregation substance of Enterococcus faecalis mediates adhesion to cultured renal tubular cells.

The sex pheromone system of Enterococcus faecalis is a unique, highly efficient plasmid collection mechanism for this species. A crucial role in this system is played by an adhesin called aggregation substance which enables the cell-cell contact between donor and recipient strains. The existence of the amino acid motif Arg-Gly-Asp-Ser in the adhesin prompted us to look for a possible binding of E. faecalis cells expressing aggregation substance to eucaryotic cells. We were able to show that the adhesin mediated binding to cultured renal tubular cells (porcine cell line LLC-PK1) via light microscopic, electron microscopic, and enzyme-linked immunosorbent assay-based studies. Synthesis of the adhesin was induced by some component(s) of serum. These data are interpreted to mean that aggregation substance is an adhesin mediating not only cell-cell contact between different E. faecalis strains but also binding of E. faecalis to eucaryotic cells, and therefore it might contribute to virulence.

Amino Acid Sequence↗

PubMed2002

Involvement of PhoP-PhoS homologs in Enterococcus faecalis virulence.

Eleven PhoP-PhoS homolog pairs were identified by searching the Enterococcus faecalis V583 genome sequence database at The Institute for Genomic Research with the Bacillus subtilis PhoP-PhoS sequences. Each pair appears to be a potential two-component system composed of a response regulator and a sensor kinase. Seven of the homologs were disrupted in E. faecalis strain OG1RF. TX10293, a mutant disrupted in one of these genes (etaR, the first gene of the gene pair designated etaRS), showed delayed killing and a higher 50% lethal dose in a mouse peritonitis model. The predicted EtaR protein sequence showed greatest similarity to LisR of Listeria monocytogenes (77%) and CsrR of Streptococcus pyogenes (70%); EtaS is 53% similar to LisK and 54% similar to CsrS. When grown in vitro, the TX10293 mutant was more sensitive to low pH (pH 3.4) and more resistant to high temperature (55 degrees C) than wild-type OG1RF. In conclusion, many potential two-component systems are identified for E. faecalis, one of which, EtaRS, was shown to be involved in stress response and virulence.

Amino Acid Sequence↗

PubMed2002

Enterococcus faecalis produces extracellular superoxide and hydrogen peroxide that damages colonic epithelial cell DNA.

Enterococcus faecalis is a commensal microorganism of the human intestinal tract that produces substantial extracellular superoxide (O(-)(2)), and derivative reactive oxygen species such as H(2)O(2) and hydroxyl radical, through autoxidation of membrane-associated demethylmenaquinone. Because these oxidants may be important as a cause of chromosomal instability (CIN) associated with sporadic adenomatous polyps and colorectal cancer, the ability of E.faecalis to damage eukaryotic cell DNA was examined using the alkaline lysis single cell gel electrophoresis (comet) assay. Both Chinese hamster ovary and HT-29 intestinal epithelial cells showed increased DNA damage after co-incubation with wild-type E. faecalis strain OG1RF, but not a transposon-inactivated mutant with attenuated extracellular O(-)(2) production. E. faecalis-mediated DNA damage was prevented by catalase, but not manganese superoxide dismutase, indicating H(2)O(2) arising from O(-)(2) was the genotoxin. In a rat model of intestinal colonization, OG1RF resulted in significantly higher stool concentrations of H(2)O(2) and 5,5-dimethyl-1-pyrroline N-oxide adducts of hydroxyl and thiyl radicals, as identified by electron spin resonance-spin trapping, compared with rats colonized with a mutant strain having attenuated O(-)(2) production. Using the comet assay, luminal cells from the colon of rats colonized with O(-)(2)-producing E. faecalis showed significantly increased DNA damage compared with control rats colonized with the mutant. These findings suggest a potentially profound role for extracellular free radical production by E. faecalis in promoting CIN associated with sporadic adenomatous polyps and colorectal cancer.

Animals↗

PubMed1991

Inactivation of metronidazole by Enterococcus faecalis.

The in-vitro inactivation of metronidazole by different clinical isolates of Enterococcus faecalis was investigated by means of association experiments in which Ent. faecalis strains and Bacteroides fragilis group strains were cultured in the same liquid medium. All of the tested Ent. faecalis strains (20 isolates) were able to protect the B. fragilis group strains against the killing effect of metronidazole at a concentration four or eight times higher than the normal MIC. Different strains of Streptococcus (14), Staphylococcus aureus (10), Staph, epidermidis (10) and Escherichia coli (8) failed to exhibit the same effect. When Ent. faecalis strains were cultured anaerobically for 24 h in the presence of 4 mg metronidazole/l, either alone or together with different B. fragilis group strains, no metronidazole could be detected subsequently in the culture supernatants by HPLC. Concomitantly an increase of four or five logs in the viable counts of the co-cultured Bacteroides strains was observed compared with Bacteroides strains cultured alone. Sonicated cell extracts of Ent. faecalis cultured either aerobically or anaerobically were found to inactivate metronidazole to the same extent, whereas the culture supernatants had no such effect.

Bacteriological Techniques↗

PubMed2006

Enterococcus faecalis: its role in root canal treatment failure and current concepts in retreatment.

Enterococcus faecalis is a microorganism commonly detected in asymptomatic, persistent endodontic infections. Its prevalence in such infections ranges from 24% to 77%. This finding can be explained by various survival and virulence factors possessed by E. faecalis, including its ability to compete with other microorganisms, invade dentinal tubules, and resist nutritional deprivation. Use of good aseptic technique, increased apical preparation sizes, and inclusion of 2% chlorhexidine in combination with sodium hypochlorite are currently the most effective methods to combat E. faecalis within the root canal systems of teeth. In the changing face of dental care, continued research on E. faecalis and its elimination from the dental apparatus may well define the future of the endodontic specialty.

Anti-Infective Agents↗

PubMed2025

The adjacent ATP-binding protein-encoding genes of the Enterococcus faecalis phosphate-specific transport (pst) locus have non-overlapping cellular functions.

UNLABELLED: The widely conserved pst-phoU operon encodes a low-velocity, high-affinity, ATP-dependent importer for inorganic phosphate (Pi). The pstB gene encodes the ATPase that powers the import of Pi into the cell. In some Firmicutes, including the gastrointestinal commensal and opportunistic pathogen Enterococcus faecalis, the pst-phoU locus contains adjacent pstB genes. In this work, we compared the functionality of E. faecalis pstB1 and pstB2. E. faecalis pstB1 and pstB2 share sequence similarities with verified PstB ATPases from Escherichia coli and Streptococcus pneumoniae and only share ~60% amino acid identity with each other. Deletion of pstB1 was associated with a growth defect in low Pi-containing chemically defined medium (CDM), reduced Pi uptake, and a moderate increase in alkaline phosphatase (AP) activity. Deletion of pstB2 fully inhibited growth in CDM regardless of inorganic phosphorus source but did not hinder growth in rich, undefined medium. The ΔpstB2 mutant also exhibited a significant increase in AP activity that was associated with extracellular Pi accumulation. Overexpression of pstB2 in the pstB1 mutant was sufficient to restore growth in low-Pi CDM, Pi uptake, and AP activity, but this was not recapitulated with overexpression of pstB1 in the ΔpstB2 mutant. Deletion of either pstB paralog increased expression of the tandem paralog, and overexpression of pstB2 in ΔpstB2 reduced pstB1 expression. These results suggest that the E. faecalis pstB2-encoded ATPase is required for Pi import, while the pstB1-encoded ATPase has an accessory role in Pi import that can be duplicated by the presence of excess PstB2. IMPORTANCE: Phosphate is critical for all microbial life. In many bacteria, inorganic phosphate (Pi) is imported by the high-affinity, low-velocity Pst-PhoU system. The pstB gene encodes the ATPase that powers Pi import. The pst-phoU operon in many Firmicutes, including the human commensal and opportunistic pathogen Enterococcus faecalis, contains adjacent pstB genes, pstB1 and pstB2. No studies on the relative biological contributions of tandem pstB paralogs in any microbe have been published. This genetic study indicates that E. faecalis pstB1 and pstB2 do not have equivalent functions. The pstB2 gene encodes an ATPase that is required for Pi import, while the ATPase encoded by pstB1 has an accessory role in Pi import that can be duplicated by the presence of excess PstB2.

Enterococcus faecalis↗

PubMed2003

Influence of Enterococcus faecalis proteases and the collagen-binding protein, Ace, on adhesion to dentin.

Enterococcus faecalis is a pathogen that persists in medicated root canals. Here, we tested the hypothesis that the E. faecalis proteases, serine protease and gelatinase, and the collagen-binding protein (Ace) contribute to adhesion to the root canal. Scanning electron microscopy was used to examine dentin binding by four E. faecalis strains: OG1RF, the wild type, and three mutant derivatives of OG1RF, TX5128, TX5243 and TX5256 deficient in serine protease and gelatinase, serine protease, and Ace, respectively. For each strain, 20 root halves were exposed to 3 x 10(9) to 5 x 10(9) cells/ml for 6 h, and 50 fields per root half were examined for adherent bacteria. Statistical analysis revealed that adherence of OG1RF was significantly greater than the mutant strains (P < 0.001), while significant differences were not detected between the protease mutants. The data indicate that serine protease and Ace aid E. faecalis binding to dentin, while the role of gelatinase is uncertain.

Analysis of Variance↗

PubMed2000

Characterization of the first clinical isolate of vancomycin-resistant Enterococcus faecalis, AH803, in Taiwan.

We previously isolated a vancomycin-resistant strain of Enterococcus faecalis, designated AH803, from the sputum of a patient with pneumonia and bacteremia in Taiwan. AH803 was resistant to vancomycin (minimal inhibitory concentration, MIC = 512 micrograms/mL) but susceptible to teicoplanin (MIC = 8 micrograms/mL), and harbored the vanA gene but not the vanB gene. In this study, we further characterized E. faecalis AH803 and the plasmid it was found to contain. DNA from AH803 was analyzed for the presence of vanA and vanB resistance genes by polymerase chain reaction. The vancomycin resistant phenotype was transferable from AH803 to E. faecalis JH2-2, at a frequency of 4.8 x 10(-2). AH803 was also resistant to gentamicin and chloramphenicol, and these antibiotic resistance phenotypes cotransferred with vancomycin resistance. The genes responsible for resistance to all three antibiotics were located on a 42-kb conjugative plasmid (pBL101). This plasmid had the same restriction enzyme digestion patterns as Tn1546, found in pIP816 of E. faecalis BM4147. Epidemiologic studies of glycopeptide resistance should perhaps combine phenotypic and genotypic methods, rather than using phenotypic methods alone.

Bacterial Proteins↗

PubMed1991

High-level gentamicin resistance in Enterococcus faecalis bacteremia.

In a retrospective analysis, patients with bacteremia due to Enterococcus faecalis with and without high-level gentamicin resistance (GRE; MIC greater than 2000 micrograms/ml) were compared. Bacteremic patients with GRE (n = 32) had significantly higher rates of nosocomial acquisition and bladder catheterization, longer hospitalizations, and more frequent prior treatment with cephalosporins than did bacteremic patients without high-level resistance (n = 19). Overall mortality was significantly associated with septic shock, high-risk source (intraabdominal, wound, respiratory tract, multiple, unknown), and polymicrobial bacteremia. Higher mortality was observed in GRE bacteremia (47%) than in bacteremia without high-level resistance (37%), but this difference was not statistically significant. For patients with monomicrobial bacteremia, low-risk source (genitourinary tract, intravascular), or treatment with antibiotics appropriate for the enterococcus, higher mortality with GRE bacteremia approached statistical significance. These results suggest that high-level resistance adversely affects survival with a pure E. faecalis bacteremia or low-risk bacteremic source. Also, response to antibiotic therapy may be diminished by high-level resistance.

Adult↗

PubMed1996

The traA gene of the Enterococcus faecalis conjugative plasmid pPD1 encodes a negative regulator for the pheromone response.

The Enterococcus faecalis conjugative plasmid pPD1 (59 kb) produces an aggregation substance in response to pheromone. The traA gene (962 bp) is a member of a gene cluster involved in the regulation of the pPD1 pheromone response. A chimeric E. faecalis suicide plasmid containing a 762-bp DNA fragment from the middle portion of the traA gene was constructed. The pPD1 traA was disrupted by integration of this chimeric plasmid via homologous recombination. The E. faecalis strain containing pPD1 with the disrupted traA exhibited dry colony morphology, constitutive clumping, and an ability to transfer at high frequencies in a short (10-min) mating period, indicating that the traA product of pPD1 is a negative regulator for the pheromone response.

Bacterial Proteins↗

PubMed2002

Identification of the Enterococcus faecalis tyrosine decarboxylase operon involved in tyramine production.

Screening of a library of Enterococcus faecalis insertional mutants allowed isolation of a mutant affected in tyramine production. The growth of this mutant was similar to that of the wild-type E. faecalis JH2-2 strain in Maijala broth, whereas high-performance liquid chromatography analyses showed that tyramine production, which reached 1,000 microg ml(-1) for the wild-type strain, was completely abolished. Genetic analysis of the insertion locus revealed a gene encoding a decarboxylase with similarity to eukaryotic tyrosine decarboxylases. Sequence analysis revealed a pyridoxal phosphate binding site, indicating that this enzyme belongs to the family of amino acid decarboxylases using this cofactor. Reverse transcription-PCR analyses demonstrated that the gene (tdc) encoding the putative tyrosine decarboxylase of E. faecalis JH2-2 is cotranscribed with the downstream gene encoding a putative tyrosine-tyramine antiporter and with the upstream tyrosyl-tRNA synthetase gene. This study is the first description of a tyrosine decarboxylase gene in prokaryotes.

Amino Acid Sequence↗

PubMed2004

Infective endocarditis from Enterococcus faecalis complicating colonoscopy in Heyde's syndrome.

A case of infective endocarditis from Enterococcus faecalis after colonoscopy in a patient with aortic stenoinsufficiency and bleeding intestinal angiodysplasia (Heyde's syndrome) is reported.A 77 year old man with aortic stenoinsufficiency presented with enterorrhagia and underwent a colonoscopy, which showed normal findings. Fifteen days later he developed a moderate degree of fever. Blood cultures were positive for E faecalis. An echocardiogram showed aortic valve vegetations, and infective endocarditis was diagnosed and successfully treated by antibiotics. Some months later, intestinal bleeding recurred and intestinal resection was performed. Histopathology showed angiodysplasia. In patients with Heyde's syndrome antibiotic prophylaxis should be considered before colonoscopy.

Aged↗

PubMed1992

Identification of new sex pheromone plasmids in Enterococcus faecalis.

We describe the identification of the following new sex pheromone plasmids in Enterococcus faecalis: a haemolysin-bacteriocin plasmid, pIP964; three R plasmids, pIP1017, pIP1438 and pIP1440; and two cryptic conjugative plasmids, pIP1141 and pMV120. The identification was based on the formation of cell aggregates on filter membranes during conjugation, on efficient transfer in broth matings, and on a positive clumping reaction of cells carrying these plasmids. In addition these plasmids hybridized with DNA probes specific for sex pheromone-induced structural genes encoding surface proteins required for conjugative transfer of the plasmids.

DNA Probes↗

PubMed1996

Clinical isolation of vancomycin-resistant Enterococcus faecalis in Taiwan.

We report the isolation of a vancomycin-resistant strain of Enterococcus faecalis, designated AH803, from a 76-year-old Taiwanese woman with pneumonia and bacteremia. This is the first documented clinical isolation of a vancomycin-resistant enterococcus in Taiwan. AH803 was repeatedly isolated from sputum specimens of the patient. AH803 had a high level of vancomycin (minimal inhibitory concentration, MIC = 512 micrograms/mL) and gentamicin (MIC > 2,000 micrograms/mL) resistance, but was susceptible to teicoplanin (MIC = 8 micrograms/mL) and ampicillin (MIC = 2 micrograms/mL). AH803 was shown by polymerase chain reaction to have the vanA gene, but not the vanB gene. Despite treatment efforts, the patient's condition continued to deteriorate. She requested to be discharged, against medical advice. The patient died at home the following day after discharge.

Aged↗

PubMed2004

Enterococcus faecalis senses target cells and in response expresses cytolysin.

Many virulent strains of Enterococcus faecalis produce a two-subunit toxin, termed cytolysin. Cytolysin expression is regulated by one of the subunits (CylL(S)'') through a quorum-sensing autoinduction mechanism. We found that when target cells are absent, the other subunit (CylL(L)'') forms a complex with CylL(S)'', blocking it from autoinducing the operon. When target cells are present, however, CylL(L)'' binds preferentially to the target, allowing free CylL(S)'' to accumulate above the induction threshold. Thus, enterococci use CylL(L)'' to actively probe the environment for target cells, and when target cells are detected, allows the organism to express high levels of cytolysin in response.

Bacterial Proteins↗

PubMed1997

Influence of gentamicin dosing interval on the efficacy of penicillin-containing regimens in experimental Enterococcus faecalis endocarditis.

The influence of the gentamicin dosing regimen was studied in experimental Enterococcus faecalis endocarditis. After inoculation, animals received penicillin, or penicillin plus once-daily gentamicin, or penicillin plus thrice-daily gentamicin, or no treatment. After the treatment period, bacterial densities within the vegetations (mean +/- SEM) were 6.06 +/- 0.30, 5.42 +/- 0.29, 4.98 +/- 0.10 and 9.97 +/- 0.16 log cfu/g for the four groups. All regimens produced significant reductions in bacterial density when compared with controls; penicillin plus thrice-daily gentamicin resulted in a significant difference from penicillin alone. Although once-daily regimens have proved effective in trials involving other organisms, such regimens do not appear to be so optimal for the treatment of enterococcal endocarditis.

Animals↗

PubMed1997

Chemical signals in gram-positive bacteria: the sex-pheromone system in Enterococcus faecalis.

This review summarizes relevant aspects of the sex-pheromone system of Enterococcus faecalis, a novel form of bacterial conjugation that plays a major role in the horizontal dissemination of genes. The process is initiated by a chemical signal, the sex pheromones, and includes several stages of interaction between the donor cell and the recipient cell. Most work in this area has focused on three plasmids, the haemolysin-bacteriocin plasmid pADI, the bacteriocin plasmid pPD1 and the Tecr (Tn125) plasmid pCF10. These plasmids share many molecular and genetic features but exhibit some interesting differences at the regulatory level. Preliminary studies suggest that many of the major components of this system may also play a role in host-parasite interactions involving enterococci.

Conjugation, Genetic↗

PubMed2000

Aggregation substance promotes adherence, phagocytosis, and intracellular survival of Enterococcus faecalis within human macrophages and suppresses respiratory burst.

The aggregation substance (AS) of Enterococcus faecalis, encoded on sex pheromone plasmids, is a surface-bound glycoprotein that mediates aggregation between bacteria thereby facilitating plasmid transfer. Sequencing of the pAD1-encoded Asa1 revealed that this surface protein contains two RGD motifs which are known to ligate integrins. Therefore, we investigated the influence of AS on the interaction of E. faecalis with human monocyte-derived macrophages which constitutively express beta(2) integrins (e.g., CD18). AS was found to cause a greater-than-fivefold increase in enterococcal adherence to macrophages and a greater-than-sevenfold increase in phagocytosis. Adherence was mediated by an interaction between the RGD motif and the integrin CD11b/CD18 (complement receptor type 3) as demonstrated by inhibition studies with monoclonal antibodies and RGD peptide. AS-bearing enterococci were significantly more resistant to macrophage killing during the first 3 h postinfection, probably due to inhibition of the respiratory burst as indicated by reduced concentrations of superoxide anion.

Bacterial Adhesion↗